2.1. Uses for Replacement Cartilage Tissue
Cartilage may be damaged by disease, such as rheumatoid or osteoarthritis, or by trauma, which can lead to serious physical deformity and debilitation. As human articular cartilage ages, its sheer compressive and tensile properties change. The superficial zone of the knee articular cartilage exhibits an increase in tensile strength up to the third decade of life, after which tensile strength decreases markedly with age as detectable damage to type II collagen occurs at the articular surface. Deep zone cartilage also exhibits a progressive decrease in tensile strength with increasing age, although collagen content does not decrease. These observations indicate that there are changes in mechanical and, hence, structural organization of cartilage with aging that, if sufficiently developed, can predispose cartilage to traumatic damage. In osteoarthritic cartilage there is excessive damage to type II collagen, resulting in crimping of collagen fibrils. In rheumatoid arthritis, the combined actions of free radicals and proteinases released from polymorpholeukocytes cause much of the damage seen at the articular surface. (Tiku et al., 1990, J. Immunol. 145:690-696). Induction of cartilage matrix degradation and proteinases by chondrocytes is probably induced primarily by interleukin-1 (IL-1) or tumor necrosis factor-.alpha. (TNF-.alpha.) (Tyler, 1985, Biochem. J. 225:493-507).
A source of replacement cartilage tissue would thus be useful in most cases of cartilage disease or trauma.